BPA and metabolic syndrome; lead and obesity; BPA and markers of cardiovascular disease // Sept 2014 Science Digest #2 (non-human & policy)

September 21, 2014 at 2:18 pm | Posted in Uncategorized | Leave a comment

Sept. 2014 Science Digest #2 //
Non-Human and Policy Research

BPA, cardiovascular disease | Adverse effects of long-term exposure to bisphenol A during adulthood leading to hyperglycaemia and hypercholesterolemia in mice . Male CD1 mice were exposed over an 8-month period to five different BPA doses below or equivalent to the current no observed adverse effect level (NOAEL). Hepatic mRNA from the animals showed an overexpression of key genes involved in cholesterol biosynthesis. BPA also induced the expression of the sterol regulatory element-binding proteins 2, a master regulator of hepatic cholesterol biosynthesis, and increased de novo cholesterol synthesis. These results are consistent with epidemiological studies reporting on a link between BPA exposure and the onset of cardiovascular diseases.

BPA, metabolic syndrome & liver disease | Perinatal exposure to bisphenol A exacerbates nonalcoholic steatohepatitis-like phenotype in male rat offspring fed on a high-fat diet. On a high-fat diet (HFD), the offspring of rats exposed to BPA showed a nonalcoholic steatohepatitis-like phenotype, characterized by extensive accumulation of lipids, large lipid droplets, profound ballooning degeneration, impaired liver function, increased inflammation, and even mild fibrosis in the liver. Perinatal exposure to BPA worsened the hepatic damage caused by the HFD in the rat offspring. The additive effects of BPA correlated with higher levels of hepatic oxidative stress.

Lead, obesity | Perinatal Lead (Pb) Exposure Results in Sex-Specific Effects on Food Intake, Fat, Weight, and Insulin Response across the Murine Life-Course. Perinatal Pb exposure at blood lead levels between 4.1 µg/dL and 32 µg/dL is associated with increased food intake, body weight, total body fat, energy expenditure, activity, and insulin response in mice. Physiological effects of developmental Pb exposure persist and vary according to sex and age.

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